Several categorizations of peripheral neuropathies exist, including one that is based on the underlying etiology. It distinguishes between entrapment and nonentrapment neuropathies. Nerve entrapment syndromes at the upper extremity typically affect the median, radial and ulnar nerves at anatomic locations where the nerve courses through nerve fibro-osseous or fibromuscular tunnels or penetrates a muscle. In cases of nerve thickening, narrowing of the tunnel or hypertrophy of the muscles, the nerve might be entrapped. Nonentrapment neuropathies include all other etiologies such as traumatic nerve injuries, inflammatory conditions, polyneuropathies and mass lesions [1, 3].

Other categorizations distinguish systemic diseases from local as well as functional diseases. Systemic diseases include ischemia, vasculitis, toxic, endocrine and metabolic disorders (e.g., diabetes), motorsensory neuropathies, amyloidosis, hyperlipidemia, multifocal motor neuropathies and inflammatory neuropathies. MRI is not expected to establish these diagnosis but may help to confirm the clinical suspicion, to show the abnormality of the involved nerves and muscles, and to document the distribution/pattern of the neuropathy [3]. Local diseases include all local abnormalities such as masses, nerve injuries, entrapment neuropathies, infections and adhesive changes following surgery. MRI has a major role in these conditions as it adds morphological information to clinical information. Imaging can show the exact localization of the lesion, and detect the underlying nerve or other pathology [3]. Functional diseases such as traction or compression mononeuritis due to habitual leg crossing or repeated typing/exercise are difficult to evaluate by MRI, as in most cases only indirect signs are visible. Dynamic assessment of peripheral nerves by the means of MRI is often not conclusive. However, ultrasound can then be an important tool to evaluate, for example, functional compressive neuropathies, since it allows dynamic or functional nerve assessment during exercise.

Peripheral nerve injuries are typically classified according to the Seddon and Sunderland classification system. In this classification system three different types of nerve injury are described, namely: neuropraxia, axonotmesis and neurotmesis [3].

Neuropraxia is the least severe type of injury. It is characterized by a predominant loss of motor function due to a temporary block of the nerve conduction. Usually there is also some degree of loss of sensory function. Neuropraxia often is associated with blunt trauma where the myelin sheaths are injured. Wallerian degeneration (a process in which the part of the axon separated from the neuron’s cell body degenerates distal to the injury) does not occur in neuropraxia. The electromyogram is usually negative. This type of injury is relatively mild and MRI of the peripheral nerve may show some abnormal increased nerve signal on fat suppressed T2-weighted magnetic resonance (MR) images, but typically no muscle denervation changes are seen [3]. Usually, there is no disruption, effacement or enlargement of the involved nerves.

Axonotmesis is a more severe type of injury and leads to axonal injury and Wallerian degeneration distal to the site of injury. Loss of both sensory and motor function occurs. Axonotmesis is characterized by axonal discontinuity and damage to the covering endoneurium. However, it is important to remember that the remaining connective tissue framework of the nerve (epineurium and perineurium) is usually preserved. As a consequence, axonotmesis injuries have the potential to recover spontaneously because the surrounding myelin sheaths remain intact. Typical clinical findings include decreased or absent evoked muscle and sensory action potentials. Electrodiagnostic tests are therefore useful for distinguishing the lower grade of injury (neuropraxia) from the more severe grade of injury (axonotmesis) [3]. Typical MRI findings include signs of muscle denervation as well as increased T2 signal intensity of the nerve on fat-suppressed images. Morphological changes can also be detected. The latter include fascicular enlargement, disruption and/or nerve effacement. Axonal regeneration occurs slowly at a rate of approximately 1 mm per day from the proximal to the distal nerve segment [3]. With advancing nerve regeneration, normalization of the abnormal T2-hyper — intensity of the nerve can be seen on MR images. The typical time frame for meaningful functional recovery is several weeks to months.

Neurotmesis is the most severe type of nerve injury, resulting from severe contusion, crush, stretch or lacerations [3]. Axonal lesions, with complete disruption of the surrounding perineurium and epineurial layers, cause complete loss of motor, sensory (and autonomic) function. In most cases, neurotmetic injuries cannot be differentiated from axonotmetic injures by means of electrodiagnosis or clinical examination. They usually do not recover because of a complete disruption of axons and connective tissue, as this makes spontaneous functional regrowth virtually impossible [3, 4]. Imaging has the potential to show a complete nerve transection in acute cases or neuroma formation in chronic cases. Although nerve conspicuity is somewhat hampered in the acute phase by hemorrhage, imaging is usually able to differentiate neurotmetic from axonotmetic injures. Longstanding muscle denervation often results in severe fatty muscle infiltration and atrophy, which severely limits the success of surgery.

Other classification systems, such as those from Sunderland et al. and Mackinnon et al., exist but discussion is beyond the scope of this syllabus.

Peripheral nerves affected by entrapment syndromes are typically compressed along their course at predisposed anatomic locations, i.e., tunnels. The floor of these tunnels usually consists of bone, whereas the roof is usually made up of focal transverse thickenings of the deep fascia, retinaculae and muscle aponeurosis [1, 3–6]. Pathophysiology of entrapment syndrome is different from other acute nerve injuries, as the development of compressive neuropathy depends on the pressure within these tunnels and the fact that nerves typically can withstand only little pressure. At more than 15 mmHg, the venous supply to the nerves is increasingly hampered, and at over 40 mmHg the arterial blood supply is affected. Irreversible structural nerve damage begins at pressures of around 80 mmHg [3]. Typical MR findings of compressed nerves include increased signal intensity on T2-weighted MR images. Recent studies have demonstrated that the large myelinated axons at the outer portions of the nerve are most affected. This relative sparing of the fibers in the central portion of the nerve supports the theory that the primary mechanism of injury is shear forces; therefore, ischemia appears to be a secondary mechanism [3]. In the early stages, symptoms can be intermittent or even disappear spontaneously. As the disease progresses, fibrotic nerve changes can occur causing further nerve impingement. In chronic cases, severe axonal degeneration and myelin loss are common histological findings. Clinically, there is a permanent loss of nerve function. Long-standing disease causes fatty infiltration and atrophy of the denervated muscles. The abnormal T2 hyperintensity of the nerve, along with proximal enlargement, angulation and displacement, are characteristic findings of nerve entrapment. Regional muscle denervation changes on MR images support the diagnosis of neuropathy.

MR neurography is a tissue-specific imaging technique optimized for evaluating peripheral nerves, their internal fascicular morphology (see above), alteration in neural signal and caliber, and associated space occupying and other compressive lesions [7]. Three-dimensional (3D) imaging is of critical importance in tracing the course of peripheral nerves, in identifying points of compression or disruption, and for preoperative planning. In general, MR neurography can be either T2 based or diffusion based. Diffusion- based MR imaging, especially diffusion tensor imaging, allows functional assessment of the nerves, but as yet remains a novel technique, with specific hardware and software requirements in an attempt to enhance the otherwise low signal-to-noise ratio (SNR) from these small nerves, limiting its application in routine clinical practice.

MR neurography is often used for the evaluation of entrapment syndromes at the upper extremity. These can affect the median and radial nerves, as well as the ulnar nerve. Detailed knowledge of the anatomy of the individual nerves is important for image interpretation, and a good text book showing the innervated muscles helps to indirectly localize the site of the nerve lesion based on the pattern of involved muscles in cases where direct visualization of the pathology is not feasible.